Post-surgery pain: what's important to know

Neuropathic pain is pain caused by damage or disease of the somatosensory nervous system. In other words, the problem lies not only in the body's tissues, but in the sensory transmission system itself: a damaged nerve, root, plexus, spinal cord, or brain begins to generate pathological pain signals. The International Association for the Study of Pain emphasizes that this is not a colloquial expression or metaphor, but a specific clinical type of pain with specific diagnostic criteria. [1]

In everyday speech, people often say "nerve pain" when they mean burning, shooting, electric shocks, tenderness to the touch, tingling, or numbness. While this description is indeed typical of neuropathic pain, it alone does not prove the diagnosis. Modern criteria require not only characteristic complaints but also a plausible connection between the symptoms and damage to the somatosensory system, followed by clinical and, if necessary, instrumental confirmation. [2]

Neuropathic pain can be peripheral or central. The peripheral form is associated with damage to the peripheral nerves, roots, sensory ganglia, or plexuses. The central form occurs with damage to structures of the brain or spinal cord. Classic examples of the peripheral form include painful diabetic polyneuropathy, postherpetic neuralgia, radiculopathy, compression and traumatic neuropathies; examples of the central form include pain after a stroke, after spinal cord injury, and in multiple sclerosis. [3]

This topic is important not only because of the intensity of the pain. Neuropathic pain often impairs sleep, mood, exercise tolerance, work ability, and overall quality of life. The International Association for the Study of Pain estimates the prevalence of neuropathic pain among adults at approximately 7%-10%, making it not a rare condition but a major clinical and social problem. [4]

Table 1. How to correctly understand the term "nerve pain"

Term	What does it mean?
Neuropathic pain	Pain caused by damage or disease of the somatosensory nervous system
Peripheral neuropathic pain	Pain due to damage to peripheral nerves, roots, ganglia, plexuses
Central neuropathic pain	Pain due to damage to the brain or spinal cord
Allodynia	Pain from a stimulus that should not normally cause pain
Hyperalgesia	Too much pain in response to a normal pain stimulus
Paresthesia	Abnormal sensations such as tingling, crawling, or crawling

Sources for the table. [5]

International Classification of Diseases and the Place of Neuropathic Pain in Coding

There's an important nuance to coding this topic: "nerve pain" isn't always coded with a single, universal code. The International Classification of Diseases, 10th Revision, includes code M79.2 for neuralgia and neuritis, unspecified, but it's only suitable for nonspecific situations. If the cause is known, it's preferable to code for the underlying condition, such as diabetic polyneuropathy, postherpetic neuralgia, radiculopathy, trigeminal nerve lesion, or sequelae of stroke. [6]

The International Classification of Diseases, 11th revision, has made the situation more logical: chronic neuropathic pain is identified as a separate category of chronic pain. Within it, a distinction is made between chronic peripheral neuropathic pain and chronic central neuropathic pain, and common clinical forms are listed, including trigeminal neuralgia, painful polyneuropathy, postherpetic neuralgia, painful radiculopathy, and pain following peripheral nerve injury. [7]

The practical implication for the editorial is simple: it is helpful to explain the general term "neuropathic pain" to the reader in the text, but in clinical documentation and medical coding, it is always better to aim for an etiologic diagnosis. This improves the accuracy of routing, assessment, and treatment. [8]

Causes and risk factors

The most common cause of peripheral neuropathy in adults is diabetes mellitus. According to reviews of peripheral neuropathy, diabetes, especially when long-term and with poor glycemic control, is the leading cause. However, painful diabetic polyneuropathy is only one form of peripheral nerve damage, and not every neuropathy in a person with diabetes is automatically attributed to diabetes alone. [9]

Important causes also include nerve compression or injury, radiculopathy, the effects of herpes zoster, toxic effects, including alcohol and certain medications, vitamin B12 deficiency, hereditary diseases, and some immune-inflammatory conditions. The International Association for the Study of Pain specifically identifies chemotherapy as a clinically significant cause of neuropathic pain. [10]

The main causes of central neuropathic pain are stroke, spinal cord injury, and certain demyelinating diseases, primarily multiple sclerosis. Here, the mechanism is different: it's not the peripheral sensory pathways that are affected, but the central structures that must correctly process the pain signal. Because of this, symptoms can coexist with other neurological disorders. [11]

Risk factors are not limited to the presence of a specific disease. The International Association for the Study of Pain notes that the likelihood of developing neuropathic pain may be higher in older people, women, people with poorer overall health, and possibly those with a genetic predisposition. For diabetic neuropathy, the duration of diabetes and the quality of glucose control are also significant. [12]

It's also important to note that some cases remain idiopathic, meaning the cause remains undetected even after a standard examination. This is not uncommon for peripheral neuropathy: according to family medicine reviews, the proportion of undiagnosed causes can reach 25%-46%. Therefore, good patient information should clearly explain that the absence of an immediately identified cause does not mean the pain is "not there" or that it is "psychological." [13]

Table 2. Common causes of neuropathic pain and typical clinical presentation

Cause	Which type of pain is more likely?	Typical drawing
Diabetes mellitus	Peripheral	Burning, tingling, pain and numbness in the feet like "socks"
Postherpetic neuralgia	Peripheral	Pain and soreness of the skin after shingles
Radiculopathy	Peripheral	Pain along the root, often with irradiation and numbness
Nerve compression or injury	Peripheral	Pain and sensory disturbances in the innervation zone of a specific nerve
Chemotherapy	Peripheral	Distal symmetrical pain, tingling, decreased sensitivity
Stroke	Central	Pain associated with central neurological damage
Spinal cord injury	Central	Pain below or around the level of the lesion, often with sensory disturbances
Multiple sclerosis	Central	Pain in combination with other focal neurological symptoms

Sources for the table. [14]

Symptoms and how neuropathic pain differs from other types of pain

The most characteristic descriptions of neuropathic pain include burning, shooting, electric shocks, stabbing and shooting sensations, a painful reaction to light touch, and a feeling of cold or heat in the painful area. Numbness, tingling, decreased sensitivity, or a "cotton wool" sensation are often present alongside the pain. These combinations are particularly significant because the coexistence of pain and sensory deficits makes a neuropathic mechanism more likely. [15]

However, no single symptom is completely specific. The updated neuropathic pain grading system emphasizes that burning, electric stabbing, pain with light touch, and numbness are suspicious but not pathognomonic. Therefore, neuropathic pain is not confirmed solely by a patient's "beautiful description." A plausible pain distribution, a clinical examination, and, if necessary, confirmatory tests are required. [16]

Classic nociceptive pain is structured differently. It occurs when tissue is damaged while the nervous system is functioning normally—for example, with joint inflammation, muscle injury, postoperative wound pain, or bruise pain. It is more typically characterized by aching, pressing, inflammatory, and mechanical pain, and is more clearly associated with movement, local inflammation, or injury.

But there's a third important mechanism: nociplastic pain. It involves a disruption in pain signal processing, but there's no clear, confirmed lesion of the somatosensory system or explanatory tissue damage. This is why modern texts must explain to readers that "nerve pain" isn't something obscure and chronic, but rather just one possible biological mechanism of pain.

In real-life practice, mixed pain is common. A person with low back pain may have both a musculoskeletal component and radiculopathy. A patient with diabetes may experience a combination of painful polyneuropathy and common joint pain in the feet. This is an important reason why treatments sometimes appear "partially effective": they may only address one of several pain mechanisms. [17]

Table 3. How to distinguish the main mechanisms of pain in practice

Sign	Neuropathic pain	Nociceptive pain	Nociplastic pain
The main mechanism	Somatosensory system damage	Tissue damage in a normal nervous system	Altered pain processing without proven nerve damage
Typical sensations	Burning, current, shooting pain, allodynia	Aching, mechanical, inflammatory pain	Diffuse, unstable, often with hypersensitivity
Numbness next to pain	Often	Usually no	Not typical
Topical correspondence to nerve anatomy	Usually there is	Not necessarily	Not necessarily
Regular painkillers	Often they help less	Work better more often	The effect is variable

Sources for the table.

When is an urgent doctor's consultation needed?

Although neuropathic pain is most often not an emergency such as a heart attack or stroke, some cases require prompt further investigation. Signs of rapid symptom progression over weeks or months, increasing weakness, hand involvement, marked asymmetry, and a predominance of motor or autonomic disturbances are cause for concern. Such signs may be associated with inflammatory, immune, or other potentially treatable but more serious neuropathies. [18]

An urgent neurological assessment is also necessary when pain is accompanied by significant gait disturbances, falls, muscle atrophy, pelvic disorders, visual or speech symptoms, or signs of cranial nerve damage. In this case, the physician must consider not only peripheral neuropathy but also damage to the central nervous system or other neurological pathology masquerading as "nerve pain." [19]

A separate group are people with diabetes and reduced sensation in their feet. Their pain may be moderate or even diminish as the sensory deficit worsens, and the main risk is associated not only with discomfort but also with injuries, ulcers, and delayed treatment. Therefore, persistent pain, numbness, a non-healing wound, a change in gait, or new sensory deficits require immediate examination. [20]

Table 4. Red flags for pain along a nerve

Sign	Why is this important?
Rapid increase in symptoms	Inflammatory or other serious neuropathy is possible.
Muscle weakness	Requires more urgent neurological evaluation
Asymmetry of symptoms	It is necessary to search for focal lesions, roots, plexuses, and compression.
Predominance of autonomic disorders	A more severe form of neuropathy is possible
Damage to the arms, hands, falls	Increases the likelihood of an atypical or progressive process
Pelvic, speech, and visual symptoms	It is necessary to exclude the central nervous system, not just the peripheral nerves

Sources for the table. [21]

Diagnostics

Diagnosis begins not with a CT scan or a long list of tests, but with a thorough medical history. The doctor clarifies the nature of the pain, its duration, rate of progression, and its relationship to previous herpes, diabetes, trauma, surgery, alcohol, medications, nutritional deficiencies, and family history. At this stage, it is important to understand whether the pain zone corresponds to the course of a nerve, root, or a typical symmetrical distal distribution. This neuroanatomical plausibility is part of the modern diagnostic confirmation system. [22]

The next step is a neurological examination. This should include testing of superficial and deep sensation, strength, reflexes, gait, and, as appropriate, signs of autonomic dysfunction. A "probable neuropathic pain" level requires not only a suspicious history but also confirmation of sensory disturbances during examination. However, the absence of obvious signs does not always completely rule out the problem, especially if small fiber tract lesions are involved. [23]

Questionnaires can be helpful, but they do not replace diagnosis. The 2023 Joint European Guidelines strongly recommend the use of the DN4, its stand-alone version, and the Leeds Neuropathic Symptoms and Signs Scale in the diagnostic workup of patients with possible neuropathic pain. The recommendation is weaker for the stand-alone version of this scale and the PainDetect scale. The main point is that the questionnaire helps identify suspected symptoms, but should not alone make a definitive diagnosis. [24]

If it is necessary to confirm not only a clinical suspicion but also the presence of damage to the somatosensory system, tests are used. For peripheral neuropathy, nerve conduction studies and needle electromyography are used, and if small fiber damage is suspected, a skin biopsy is particularly valuable, for which European guidelines strongly recommend. Quantitative sensory testing and evoked potentials can be used additionally, but the level of evidence for these is weaker. Functional neuroimaging and nerve blocks are useful for understanding the mechanism or prognosis, but are not recommended as a diagnostic tool for confirming neuropathic pain. [25]

A laboratory investigation of the cause is essential, at least at a basic level. Reviews of peripheral neuropathy recommend starting with a complete blood count, biochemical profile, fasting glucose, vitamin B12 levels, thyroid-stimulating hormone, and serum protein electrophoresis with immunofixation. If the initial evaluation fails to explain the symptoms or if the course of the disease is alarming, the patient is referred to a neurologist for a more in-depth diagnosis, including additional tests, antibodies, and, less commonly, nerve biopsy and pinpoint imaging. [26]

It is important to remember that magnetic resonance imaging (MRI) is not automatically necessary for all patients with suspected peripheral neuropathy. It is usually ineffective in isolated, typical, length-dependent sensory neuropathy. MRI is more appropriate when polyradiculopathy, plexopathy, atypical neuropathy, or central nervous system involvement are suspected. [27]

Table 5. What is used in diagnostics and why

Method	What is it for?	Comment
History and topic of pain	Understand whether the pain follows a nerve path or a typical neuropathy pattern	The basis of diagnostics
Neurological examination	Check sensitivity, strength, reflexes, gait	Needed to move from “possible” to “probable” pain
DN4 questionnaires and the Leeds scale	Identify neuropathic signs	They help, but they don’t replace a diagnosis.
Nerve conduction studies and needle electromyography	Confirm peripheral nerve damage and specify the type of damage	Especially useful for large fibers
Skin biopsy	Confirm fine fiber damage	Has a strong recommendation in specialized diagnostics
Laboratory tests	Find a treatable cause	Glucose, vitamin B12, thyroid-stimulating hormone, protein fractions, and others
Magnetic resonance imaging	Localize the atypical lesion	It is not a routine test for everyone.

Sources for the table. [28]

Treatment

Treatment for neuropathic pain always involves two approaches. First, eliminating or correcting the underlying cause is crucial: improving diabetes control, discontinuing or replacing a toxic medication, correcting vitamin B12 deficiency, treating inflammation or compression, or addressing the consequences of a herpes infection or injury. Second, reducing the pain itself and its impact on sleep, mood, daily activities, and performance. Symptomatic therapy alone, without identifying the underlying cause, is often incomplete. [29]

For general adult care, the UK's National Institute for Health and Care Excellence recommends amitriptyline, duloxetine, gabapentin, or pregabalin as initial pharmacotherapy for all types of neuropathic pain except trigeminal neuralgia. If the first drug is ineffective or poorly tolerated, a switch to one of the remaining options is suggested. Tramadol is considered only as a short-term "rescue" therapy, and for localized pain, capsaicin cream may be used in people who do not want or cannot tolerate oral medications. [30]

Trigeminal neuralgia is a special case. For it, the same British document recommends starting with carbamazepine, as it is a clinically distinct form of neuropathic pain with its own evidence base and treatment logic. This is an important clarification, as the general treatment guidelines for "ordinary" peripheral neuropathic pain do not apply here without reservations. [31]

For painful diabetic polyneuropathy, the American Academy of Neurology recommends a broader range of effective classes: tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, gabapentinoids, and sodium channel blockers. However, drug selection should consider not only efficacy but also comorbidities, cost, patient preference, and side effect profile. This means that for one person, duloxetine may be the best choice, for another, pregabalin, and for a third, amitriptyline or another suitable class. [32]

A realistic discussion about treatment goals is essential. The American Academy of Neurology emphasizes that the goal of therapy is to reduce, not necessarily eliminate, pain. If a drug has been titrated to an effective dose and has not produced clinically significant improvement after approximately 12 weeks, or if the side effects outweigh the benefits, the therapy is considered unsuccessful and a different class is tried. [33]

Opioids are no longer considered a standard treatment option. The American Academy of Neurology's guidelines explicitly state that opioids should not be used to treat painful diabetic polyneuropathy, and tramadol and tapentadol are also not recommended as a standard long-term strategy. This shift is important for this article because it reflects a shift away from short-term analgesia toward safer and more long-term management. [34]

A large international review from 2025 broadened the picture slightly for specialty practice. It supported a strong recommendation for tricyclic antidepressants, alpha-2-delta ligands, and serotonin-norepinephrine reuptake inhibitors as first-line therapy, a weak recommendation for 8% capsaicin patches, capsaicin cream, and 5% lidocaine patches as second-line therapy, and a weak recommendation for botulinum toxin type A, repetitive transcranial magnetic stimulation, and opioids as third-line therapy. This does not contradict the UK guidelines, but rather highlights the difference between entry-level care in general practice and the expanded capabilities of specialist pain centers. [35]

Non-pharmacological measures are also important. The American Academy of Neurology's guidelines for diabetic polyneuropathy recommend the use of exercise, cognitive-behavioral approaches, mindfulness practices, and tai chi as adjunctive measures in some patients. Furthermore, in people with neuropathic pain, it is important to separately assess and treat concomitant sleep and mood disorders, as they significantly impact both pain perception and overall treatment outcome. [36]

Table 6. Modern logic of treatment of neuropathic pain

Stage	What do they usually do?	What do they pay attention to?
1	Confirm the mechanism of pain and look for the cause	Without this, it is easy to treat the wrong mechanism.
2	Correct reversible causes	Glycemia, vitamin B12 deficiency, toxic drugs, nerve compression
3	Selecting initial therapy	Amitriptyline, duloxetine, gabapentin, pregabalin; for trigeminal neuralgia carbamazepine
4	The drug class is changed if it is ineffective or poorly tolerated.	Don't keep increasing the dose of a drug that doesn't work.
5	Local and specialized therapy are considered	Capsaicin, lidocaine, botulinum toxin type A, neuromodulation as indicated
6	At the same time, they treat sleep, anxiety, depression, and activity limitation.	This improves the overall outcome of treatment.

Sources for the table. [37]

Prevention and prognosis

The prognosis depends primarily on the cause. In some people, neuropathic pain improves over time or with treatment, but in others, it becomes chronic and requires long-term management. The International Association for the Study of Pain clearly emphasizes that the course of pain varies greatly: there is no single scenario for all patients. [38]

The best prevention is to prevent the progression of diseases that damage nerves. For diabetes, this means good disease management and regular assessment of symptoms, pain, function, and quality of life. For other conditions, this means reducing exposure to alcohol and toxins, being mindful of medications that can damage nerves, correcting vitamin B12 deficiency, and seeking early treatment for compressive and inflammatory neuropathies. [39]

With peripheral neuropathy, it's important not to focus solely on the pain. Decreased foot sensation increases the risk of injury, burns, calluses, and ulcers. Therefore, prevention includes education, regular foot examinations, skin protection, properly fitted shoes, and avoiding the habit of ignoring numbness simply because it "doesn't hurt as much." [40]

Even in chronic cases, the treatment goal remains achievable: reducing pain intensity, improving sleep, mobility, mood, and the ability to perform daily activities. In modern neurology and pain medicine, this is considered a complete therapeutic success, even if complete symptom resolution does not occur. [41]

Frequently Asked Questions

Is it possible to immediately understand by the sensation that it is nerve pain?

No. Burning, shooting, electric shocks, and tenderness to touch make neuropathic pain probable, but they alone do not prove it. Clinical logic, examination, and sometimes confirmatory tests are needed. [42]

If there is numbness, is it always neuropathy?

No, that's not true. Numbness often accompanies neuropathic pain, but it can also occur with other neurological conditions. It's not just the presence of numbness that's important, but also its distribution, rate of development, association with weakness, and examination findings. [43]

Does everyone need an EMG?

While it may be useful for many patients with unclear peripheral neuropathy, it is especially important when it comes to confirming large-fiber lesions and clarifying the location, type, and severity of the process. However, some small-fiber lesions may require other methods, including skin biopsy. [44]

Is it true that regular painkillers hardly help?

For neuropathic pain, conventional analgesics are often less effective than for ordinary tissue pain. Therefore, the basis of treatment usually consists of medications that affect pain signaling in the nervous system, rather than the standard "simply relieve pain" approach.

Can neuropathic pain be completely cured?

Sometimes, yes, especially if a reversible cause is quickly addressed. But in many cases, the goal of treatment is to significantly reduce pain and improve function, not to completely and immediately eliminate symptoms. Current guidelines recommend discussing this honestly with the patient immediately. [45]

Why does one drug help and another doesn’t?

Because neuropathic pain is heterogeneous. The cause, anatomical level of damage, involved fibers, associated anxiety and sleep disturbances, and drug tolerance and sensitivity vary among individuals. Therefore, treatment selection often proceeds in stages, with transitions between drug classes. [46]

Key points from experts

Nanna Brix Finnerup, Professor of Clinical Medicine and Director of the Danish Pain Research Centre at Aarhus University, is involved in the development of the international NeuPSIG guidelines and the 2025 review of neuropathic pain treatment. The practical implication of this line of research is that neuropathic pain requires stepwise, mechanism-oriented treatment rather than a one-size-fits-all approach to pain relief. [47]

Andrea Truini, Professor in the Department of Human Neurosciences at Sapienza University in Rome and lead author of the 2023 joint European guidelines for the diagnosis of neuropathic pain, explains the main diagnostic principle: questionnaires are useful, but the final decision should be based on clinical examination and confirmation of damage to the somatosensory system, and not only on the patient's complaints. [48]

Simon Harutyunyan, an associate professor of anesthesiology and director of clinical translational research and clinical trials at the Washington University Pain Center in St. Louis, is among the authors of the 2025 international review. His research position reflects the current view on the problem well: neuropathic pain is heterogeneous, so personalized treatment selection is more important than mechanically prescribing one “standard” drug to all patients. [49]

Raymond S. Price, professor of clinical neurology at the University of Pennsylvania and co-author of the updated American Academy of Neurology guidelines on painful diabetic polyneuropathy, emphasizes two practical ideas: assessing not only the pain itself but also its impact on function and quality of life, and explaining to patients upfront that the goal of treatment is often to significantly reduce pain rather than eliminate it completely. [50]